Multisite phosphorylation by Cdk1 initiates delayed negative feedback to control mitotic transcription

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TLE4 acts as a corepressor of Hes1 to inhibit inflammatory responses in macrophages

Macrophages play a key role in maintaining homeostasis and in mounti ng compete nt immune responses.Upon stimulation,one of the key effector functions of activated macrophages is production of inflammatory cytokines including interleukin 6(IL-6)and interleukin 12(IL-12).IL-6 and IL-12 are important for transition from innate to adaptive immunity,and thus essential for host defense against multiple pathogens(Kishimoto,2005;Trinchieri,2003).     

Mapping the transcription site of the SV40-specific late 16 S mRNA.

This paper describes the purification of polysomal RNA from SV40-lytically infected CV1 (monkey) cells and separation of the two distinct classes of SV40-specific mRNA sedimenting at 16 S and 19 S. These classes have been hybridized with the whole SV40 DNA genome as well as with the SV40 Hind fragments. The results have permitted the mapping of SV40-specific late 16 S mRNA from approximately 0.945 to 0.175 map units.     

An antigen expressed in proliferating cells at late G1-S phase

A monoclonal antibody Pr-28 was prepared, which recognized an antigen present only in proliferating cells. Immunofluorescence analysis of Pr-28 antigen showed that the antigen was localized mainly in perinuclear cytoplasm. Although Pr-28 antibody was produced against a chicken cell antigen, it reacts not only with chicken cells but also other cells of murine origin, such as L-cells and NIH 3T3 cells. The molecular weight (Mr) of the antigen recognized by Pr-28 antibody was 45,000 D as determined by SDS-PAGE run under reducing conditions. The antigen disappeared in NIH 3T3 quiescent cells, reappearing in quiescent cells stimulated by fetal calf serum (FCS). The synthesis of Mr 45,000 protein occurred at late G1 phase, just before DNA synthesis in serum-stimulated quiescent NIH 3T3 cells and ceased in S phase.     

Sp1-like protein KLF13 acts as a negative feedback regulator of TGF-β signaling and fibrosis

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